Background. The NT-ProBNP/BNP test has been validated as a marker for determining the etiology of acute dyspnea. In the setting of end-stage renal disease on hemodialysis (ESRD on HD), the utility of the NT-ProBNP/BNP test has not been validated. This study examines the clinical utility of the NT-ProBNP test in the setting of ESRD on HD patients presenting with acute dyspnea. Methods. A retrospective case series of 250 subjects were admitted to Cooper University Hospital, 07/2010-03/2011, with ESRD and HD presenting with dyspnea. The incidences of echocardiography, cardiology consultation, and NT-ProBNP elevated and normal were examined. Correlation coefficients were calculated for NT-ProBNP with age (years), estimated dry weight (kg), amount of fluid removed (L), and ejection fraction (EF in %) among other echocardiography parameters. Results. Of the total sample 235 patients had NT-ProBNP levels performed. Cardiology consults were placed in 68.8% and 58% who underwent echocardiography. Of those for whom an echocardiography was performed estimated mean EFs of 54.6%, 50.8%, and 61.7% were observed among the NT-ProBNP elevated group, normal group, and no NT-ProBNP group, respectively. No differences were detected in all other echocardiography measurements. No correlation was observed between NT-ProBNP and age ( ), baseline EDW ( ), amount of fluid removed ( ), or EF ( ). Conclusion. In the setting of ESRD on HD, the NT-ProBNP test has no clinical utility in determining the etiology of acute dyspnea. This can be demonstrated through echocardiographic and therapeutic parameters measured in this study. 1. Introduction Both N-Terminus Pro Brain Natriuretic Peptide (NT-ProBNP) and Brain Natriuretic Peptide (BNP) hormones have been used in patients presenting with a chief complaint of dyspnea to predict whether Left Ventricular Systolic Dysfunction (LVSD) is causative for this symptom. The breathing not properly data and studies by Morrison, et al. demonstrated a high positive predictive value (PPV) for predicting congestive heart failure as the etiology of patients presenting with dyspnea to the emergency department [1–5]. The sensitivity and specificity of the BNP assay has been reported to be high, if serum concentrations are greater than 100 picograms per milliliter (pg/mL) for BNP and 500？pg/mL for NT-ProBNP for predicting LVSD as the etiology of dyspnea [6, 7]. Thus with a high pretest probability, members of the emergency department utilize the NT-ProBNP and BNP in the decision tree to treat patients presenting with dyspnea. The presence of chronic
References
[1]
L. K. Morrison, A. Harrison, P. Krishnaswamy, R. Kazanegra, P. Clopton, and A. Maisel, “Utility of a rapid B-natriuretic peptide assay in differentiating congestive heart failure from lung disease in patients presenting with dyspnea,” Journal of the American College of Cardiology, vol. 39, no. 2, pp. 202–209, 2002.
[2]
P. A. McCullough, J. E. Hollander, R. M. Nowak et al., “Uncovering heart failure in patients with a history of pulmonary disease: rationale for the early use of B-type natriuretic peptide in the emergency department,” Academic Emergency Medicine, vol. 10, no. 3, pp. 198–204, 2003.
[3]
Q. Dao, P. Krishnaswamy, R. Kazanegra, et al., “Utility of B-Type Natriuretic Peptide (BNP) in the diagnosis of CHF in an urgent care setting,” Journal of the American College of Cardiology, vol. 37, pp. 379–385, 2001.
[4]
M. Davis, E. Espiner, G. Richards, et al., “Plasma brain natriuretic peptide in assessment of acute dyspnea,” The Lancet, vol. 343, pp. 440–444, 1994.
[5]
A. Maisel, P. Krishnaswamy, R. M. Nowak, et al., “Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure,” The New England Journal of Medicine, vol. 347, no. 3, pp. 161–167, 2002.
[6]
A. Strunk, V. Bhalla, P. Clopton et al., “Impact of the history of congestive heart failure on the utility of B-type natriuretic peptide in the emergency diagnosis of heart failure: results from the breathing not properly multinational study,” American Journal of Medicine, vol. 119, no. 1, pp. 69.e1–69.e11, 2006.
[7]
C. K. Brenden, J. E. Hollander, D. Guss et al., “Gray zone BNP levels in heart failure patients in the emergency department: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study,” American Heart Journal, vol. 151, no. 5, pp. 1013–1018, 2006.
[8]
J. Pimenta, F. Sampaio, P. Martins et al., “Aminoterminal B-type natriuretic peptide (NT-proBNP) in end-stage renal failure patients on regular hemodialysis: does it have diagnostic and prognostic implications?” Nephron—Clinical Practice, vol. 111, no. 3, pp. c182–c188, 2009.
[9]
L. Sun, Y. Sun, X. Zhao, et al., “Predictive role of BNP and NT-proBNP in hemodialysis patients,” Nephron Clinical Practice, vol. 110, no. 3, pp. c178–c184, 2008.
[10]
S. Anwaruddin, D. M. Lloyd-Jones, A. Baggish et al., “Renal function, congestive heart failure, and amino-terminal pro-brain natriuretic peptide measurement: results from the ProBNP investigation of dyspnea in the emergency department (PRIDE) study,” Journal of the American College of Cardiology, vol. 47, no. 1, pp. 91–97, 2006.
[11]
C. R. DeFilippi, S. L. Seliger, S. Maynard, and R. H. Christenson, “Impact of renal disease on natriuretic peptide testing for diagnosing decompensated heart failure and predicting mortality,” Clinical Chemistry, vol. 53, no. 8, pp. 1511–1519, 2007.
[12]
C. Bruch, H. Reinecke, J. Stypmann et al., “Impact of renal disease on natriuretic peptide testing for diagnosing decompensated heart failure and predicting mortality,” Journal of Heart and Lung Transplantation, vol. 25, no. 9, pp. 1135–1141, 2006.
[13]
S. Dhar, G. S. Pressman, S. Subramanian et al., “Natriuretic peptides and heart failure in the patient with chronic kidney disease: a review of current evidence,” Postgraduate Medical Journal, vol. 85, no. 1004, pp. 299–302, 2009.
[14]
J. Racek, H. Králová, L. Trefil, D. Rajdl, and J. Eiselt, “Brain natriuretic peptide and N-terminal proBNP in chronic haemodialysis patients,” Nephron—Clinical Practice, vol. 103, no. 4, pp. c162–c172, 2006.
[15]
A. Y. Wang, C. W. Lam, C. M. Yu, et al., “N-terminal pro-brain natri- uretic peptide: an independent risk predictor of cardiovascular con- gestion, mortality, and adverse cardiovascular outcomes in chronic peritoneal dialysis patients,” Journal of the American Society of Nephrology, vol. 18, pp. 321–330, 2007.
[16]
I. A. Khan, J. Fink, C. Nass, H. Chen, R. Christenson, and C. R. deFilippi, “N-terminal pro-brain natri- uretic peptide: an independent risk predictor of cardiovascular con- gestion, mortality, and adverse cardiovascular outcomes in chronic peritoneal dialysis patients,” American Journal of Cardiology, vol. 97, no. 10, pp. 1530–1534, 2006.
[17]
R. M. Lang, M. Bierig, R. B. Devereux et al., “Recommendations for chamber quantification: a report from the American Society of Echocardiography's guidelines and standards committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology,” Journal of the American Society of Echocardiography, vol. 18, no. 12, pp. 1440–1463, 2005.
[18]
M. A. Quinones, A. D. Waggoner, and L. A. Reduto, “A new simplified and accurate method for determining ejection fraction with two-dimensional echocardiography,” Circulation, vol. 64, no. 4, pp. 744–753, 1981.
[19]
J. P. Henry and J. W. Pearce, “The possible role of cardiac atrial stretch receptors in the induction of changes in urine flow,” The Journal of Physiology, vol. 131, no. 3, pp. 572–585, 1956.
[20]
R. Klinge, M. Hystad, J. Kjekshus, et al., “An experimental study of cardiac natriuretic peptides as markers of development of CHF,” Scandinavian Journal of Clinical & Laboratory Investigation, vol. 58, pp. 683–691, 1998.
[21]
K. Hosoda, K. Nakao, M. Mukoyama et al., “Expression of brain natriuretic peptide gene in human heart: production in the ventricle,” Hypertension, vol. 17, no. 6, pp. 1152–1155, 1991.
[22]
W. J. Austin, V. Bhalla, I. Hernandez-Arce et al., “Correlation and prognostic utility of B-type natriuretic peptide and its amino-terminal fragment in patients with chronic kidney disease,” American Journal of Clinical Pathology, vol. 126, no. 4, pp. 506–512, 2006.
[23]
K. S. Spanaus, F. Kronenberg, E. Ritz et al., “B-type natriuretic peptide concentrations predict the progression of nondiabetic chronic kidney disease: the mild-to-moderate kidney disease study,” Clinical Chemistry, vol. 53, no. 7, pp. 1264–1272, 2007.
[24]
J. Pimenta, F. Sampaio, P. Martins et al., “Aminoterminal B-type natriuretic peptide (NT-proBNP) in end-stage renal failure patients on regular hemodialysis: does it have diagnostic and prognostic implications?” Nephron—Clinical Practice, vol. 111, no. 3, pp. c182–c188, 2009.
[25]
M. H. Rosner, “Measuring risk in end-stage renal disease: is N-terminal pro brain natriuretic peptide a useful marker?” Kidney International, vol. 71, no. 6, pp. 481–483, 2007.
[26]
L. H. Madsen, S. Ladefoged, P. Corell, M. Schou, P. R. Hildebrandt, and D. Atar, “N-terminal pro brain natriuretic peptide predicts mortality in patients with end-stage renal disease in hemodialysis,” Kidney International, vol. 71, no. 6, pp. 548–554, 2007.
[27]
S. Satyan, R. P. Light, and R. Agarwal, “Relationships of N-terminal pro-B-natiuretic peptide and cardiac troponin T to left ventricular mass and function and mortality in asymptomatic hemodialysis patients,” American Journal of Kidney Diseases, vol. 50, no. 6, pp. 1009–1019, 2007.
